Gastritis and B-cell clonal expansion in Sjogren's syndrome. Role of Helicobacter pylori and other infectious agents

Patients with Sjogren's syndrome often complain of epigastric pain and dyspepsia. The associated gastritis appears to result from an endogenous, likely autoimmune, component to which H. pylori infection is often superimposed. Frequently, anti-gastric mucosa autoantibodies are present in serum. The latter are often associated with H. pylori infection and gastric atrophy. Preliminary observations suggest that HCV may act like H. pylori, providing an antigenic stimulus for lymphocyte proliferation, MALT formation and B-cell clonal expansion. Mucosa Associated Lymphoid Tissue (MALT) lymphoma may arise as a result of the combination between the underlying B-cell disorder and a protracted stimulation by a local trigger. Sjogren's syndrome may represent an excellent model to dissect individual predisposing factors from local infection in the development of gastric mucosal damage.